ArticleActa physiologica (Oxford, England)2007
Separation of early afterdepolarizations from arrhythmogenic substrate in the isolated perfused hypokalaemic murine heart through modifiers of calcium homeostasis.
Article in Acta physiologica (Oxford, England), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Arrhythmic Risk Assessment of Hypokalaemia Using Human Pluripotent Stem Cell-Derived Cardiac Anisotropic Sheets.Frontiers in cell and developmental biology · 2021Article
- Arrhythmogenic Mechanisms in Hypokalaemia: Insights From Pre-clinical Models.Frontiers in cardiovascular medicine · 2021Review
- Immediate and Delayed Response of Simulated Human Atrial Myocytes to Clinically-Relevant Hypokalemia.Frontiers in physiology · 2021Article
- Genetic Loss ofCirculation. Arrhythmia and electrophysiology · 2020Article
- Hypokalemia-Induced Arrhythmias and Heart Failure: New Insights and Implications for Therapy.Frontiers in physiology · 2018Review
- Age-dependent atrial arrhythmic phenotype secondary to mitochondrial dysfunction in Pgc-1β deficient murine hearts.Mechanisms of ageing and development · 2017Article
- Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Physiological reviews · 2017Review
- Molecular Basis of Hypokalemia-Induced Ventricular Fibrillation.Circulation · 2015Article
- Small-Conductance Calcium-Activated Potassium Current Is Activated During Hypokalemia and Masks Short-Term Cardiac Memory Induced by Ventricular Pacing.Circulation · 2015Article
- Nonequilibrium reactivation of Na+ current drives early afterdepolarizations in mouse ventricle.Circulation. Arrhythmia and electrophysiology · 2014Article
- Cardiac electrophysiology in mice: a matter of size.Frontiers in physiology · 2012Article
- Empirical correlation of triggered activity and spatial and temporal re-entrant substrates with arrhythmogenicity in a murine model for Jervell and Lange-Nielsen syndrome.Pflugers Archiv : European journal of physiology · 2009Article
- Arrhythmogenic actions of the Ca2+ channel agonist FPL-64716 in Langendorff-perfused murine hearts.Experimental physiology · 2009Article
- Effects of potassium channel openers in the isolated perfused hypokalaemic murine heart.Acta physiologica (Oxford, England) · 2008Article
- Pharmacological separation of early afterdepolarizations from arrhythmogenic substrate in DeltaKPQ Scn5a murine hearts modelling human long QT 3 syndrome.Acta physiologica (Oxford, England) · 2008Article
- Restitution analysis of alternans and its relationship to arrhythmogenicity in hypokalaemic Langendorff-perfused murine hearts.Pflugers Archiv : European journal of physiology · 2008Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
aimsWe resolved roles for early afterdepolarizations (EADs) and transmural gradients of repolarization in arrhythmogenesis in Langendorff-perfused hypokalaemic murine hearts paced from the right ventricular epicardium.
methodsLeft ventricular epicardial and endocardial monophasic action potentials (MAPs) and arrhythmogenic tendency were compared in the presence and absence of the L-type Ca(2+) channel blocker nifedipine (10 nm-1 microm) and the calmodulin kinase type II inhibitor KN-93 (2 microm).
resultsAll the hypokalaemic hearts studied showed prolonged epicardial and endocardial MAPs, decreased epicardial-endocardial APD(90) difference, EADs, triggered beats and ventricular tachycardia (VT) (n = 6). In all spontaneously beating hearts, 100 (but not 10) nm nifedipine reduced both the incidence of EADs and triggered beats from 66.9 +/- 15.7% to 28.3 +/- 8.7% and episodes of VT from 10.8 +/- 6.3% to 1.2 +/- 0.7% of MAPs (n = 6 hearts, P < 0.05); 1 microm nifedipine abolished all these phenomena (n = 6). In contrast programmed electrical stimulation (PES) still triggered VT in six of six hearts with 0, 10 and 100 nm but not 1 microm nifedipine. 1 microm nifedipine selectively reduced epicardial (from 66.1 +/- 3.4 to 46.2 +/- 2.5 ms) but not endocardial APD(90), thereby restoring DeltaAPD(90) from -5.9 +/- 2.5 to 15.5 +/- 3.2 ms, close to normokalaemic values. KN-93 similarly reduced EADs, triggered beats and VT in spontaneously beating hearts to 29.6 +/- 8.9% and 1.7 +/- 1.1% respectively (n = 6) yet permitted PES-induced VT (n = 6), in the presence of a persistently negative DeltaAPD(90).
conclusionsThese findings empirically implicate both EADs and triggered beats alongside arrhythmogenic substrate of DeltaAPD(90) in VT pathogenesis at the whole heart level.
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